Mighty is a novel promyogenic factor in skeletal myogenesis

Marshall, Amy D.; Salerno, Mônica Senna; Thomas, Mark; Davies, Todd John; Berry, Carole; Dyer, Kelly A.; Bracegirdle, Jeremy; Watson, Trevor; Dziadek, Marie; Kambadur, Ravi; Bower, Rob; Sharma, Mridula

doi:10.1016/j.yexcr.2008.01.004

Cited by 83 publications

(122 citation statements)

References 43 publications

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“…A second, more direct evidence for the potential effects of lower myostatin expression after Dex treatment comes from a paper by Marshall and colleagues (41). A novel gene, Mighty, was found to be significantly upregulated in the skeletal muscle of myostatin-KO mice.…”

Section: Discussionmentioning

confidence: 99%

“…A novel gene, Mighty, was found to be significantly upregulated in the skeletal muscle of myostatin-KO mice. Analysis of the Mighty gene promoter suggested that myostatin represses Mighty expression at the transcriptional level (41). In vitro, Mighty overexpression enhanced cell differentiation with the expression of myogenic factors, while in vivo it increased muscle fiber size.…”

Section: Discussionmentioning

confidence: 99%

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Expression profiling of skeletal muscle in young bulls treated with steroidal growth promoters

Carraro¹,

Ferraresso²,

Cardazzo³

et al. 2009

Physiological Genomics

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Dexamethasone (Dex), alone or in association with estrogens, is often illegally administered per os at very low dosage as a growth promoter in beef cattle, with effects that are opposite to the muscle wasting and atrophy induced by repeated administration at therapeutic dosages. In vitro and in vivo studies have investigated the catabolic effects of Dex at therapeutic doses on skeletal muscle, demonstrating an increase in the expression of GDF8 (myostatin) gene, a well-known negative regulator of skeletal muscle mass, in a dose-dependent way. This suggested a direct role of myostatin in Dex-induced muscle wasting. In the present study, an oligonucleotide microarray platform was used to compare expression profiles of beef cattle muscle in animals treated with either Dex or Dex plus 17-β estradiol (Estr) administered at subtherapeutic dosage, against untreated controls. Data analysis demonstrates that the expression profiles were strongly affected by Dex treatment with hundreds of genes upregulated with relevant fold-change, whereas seven genes were downregulated including the myostatin gene. On the contrary, the number of differentially regulated genes was lower in response to the addition of Estr to the Dex treatment. Differentially regulated genes were analyzed to describe the effects of these treatments on muscle physiology, highlighting the importance of specific pathways (e.g., Wnt or cytokine signaling) and cellular processes (e.g., cell shape and motility). Finally, the observed differences in the expression profile will allow the development of indirect bio-markers to detect illegal Dex treatments in beef cattle using quantitative RT-PCR.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression profiling of skeletal muscle in young bulls treated with steroidal growth promoters

Carraro¹,

Ferraresso²,

Cardazzo³

et al. 2009

Physiological Genomics

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“…Akirins are essential in animal development, owing to the lethal embryonic phenotype of mice knockouts as well as the lethal or reduced growth phenotypes demonstrated by targeted knockdown in Drosophila, ticks, and nematodes (de la Fuente et al, 2006;Goto et al, 2008;Maeda et al, 2001). Meanwhile, akirins participate in regulating gene expressions in numerous physiological processes, including the innate immune responses of mammalians and insects (Goto et al, 2008;Tartey et al, 2014), metazoan myogenesis (Marshall et al, 2008;Salerno et al, 2009), mammalian carcinogenesis (Komiya et al, 2008), insect reproduction, and arthropod growth (Almazán et al, 2005;de la Fuente et al, 2006de la Fuente et al, , 2008. Furthermore, the study demonstrated that akirins are required to activate a subset of Relish-dependent genes (Bonnay et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Evolution of akirin family in gene and genome levels and coexpressed patterns among family members and rel gene in croaker

Liu

Gao

2015

Developmental & Comparative Immunology

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“…Akirins are found in diverse animal species and possess two conserved regions at their N and C termini, the former containing a nuclear localization signal, and have been reported to be crucial for regulating gene expression in a wide range of contexts (21)(22)(23)(24)(25). It has also been established that Akirin has a promyogenic role during muscle regeneration in mice (26). There are two Akirin family members in humans and mice.…”

mentioning

confidence: 99%

Essential Function for the Nuclear Protein Akirin2 in B Cell Activation and Humoral Immune Responses

Tartey

Matsushita

Imamura

et al. 2015

The Journal of Immunology

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Akirin2, an evolutionarily conserved nuclear protein, is an important factor regulating inflammatory gene transcription in mammalian innate immune cells by bridging the NF-κB and SWI/SNF complexes. Although Akirin is critical for Drosophila immune responses, which totally rely on innate immunity, the mammalian NF-κB system is critical not only for the innate but also for the acquired immune system. Therefore, we investigated the role of mouse Akirin2 in acquired immune cells by ablating Akirin2 function in B lymphocytes. B cell–specific Akirin2-deficient (Cd19Cre/+Akirin2fl/fl) mice showed profound decrease in the splenic follicular (FO) and peritoneal B-1, but not splenic marginal zone (MZ), B cell numbers. However, both Akirin2-deficient FO and MZ B cells showed severe proliferation defect and are prone to undergo apoptosis in response to TLR ligands, CD40, and BCR stimulation. Furthermore, B cell cycling was defective in the absence of Akirin2 owing to impaired expression of genes encoding cyclin D and c-Myc. Additionally, Brg1 recruitment to the Myc and Ccnd2 promoter was severely impaired in Akirin2-deficient B cells. Cd19Cre/+Akirin2fl/fl mice showed impaired in vivo immune responses to T-dependent and -independent Ags. Collectively, these results demonstrate that Akirin2 is critical for the mitogen-induced B cell cycle progression and humoral immune responses by controlling the SWI/SNF complex, further emphasizing the significant function of Akirin2 not only in the innate, but also in adaptive immune cells.

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Mighty is a novel promyogenic factor in skeletal myogenesis

Cited by 83 publications

References 43 publications

Expression profiling of skeletal muscle in young bulls treated with steroidal growth promoters

Expression profiling of skeletal muscle in young bulls treated with steroidal growth promoters

Evolution of akirin family in gene and genome levels and coexpressed patterns among family members and rel gene in croaker

Essential Function for the Nuclear Protein Akirin2 in B Cell Activation and Humoral Immune Responses

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